An up-regulation of renal α2A-adrenoceptors is associated with resistance to salt-induced hypertension in Sabra rats

被引:0
|
作者
Khalid, M [1 ]
Giudicelli, Y [1 ]
Dausse, JP [1 ]
机构
[1] Univ Paris 05, Fac Med Paris Ouest, Dept Biochem & Mol Biol, Paris, France
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中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
This study investigates the incidence of high-salt diet in blood pressures, renal alpha (2)-adrenoceptor subtypes distribution, and gene expression in salt-sensitive (SBH) and salt-resistant (SBN) Sabra rats. Comparisons have been made between SBH and SBN rats submitted to a normal or a high-salt diet for 6 weeks. Only alpha B-2-adrenoceptors are detected in kidneys of SBH rats, whatever the diet. In contrast, mRNA corresponding to alpha (2)A- and alpha B-2-subtypes are found in this substrain. In these rats, high-salt diet increases blood pressures and up-regulates gene expression and density of only alpha B-2-adrenoceptors. Inversely, alpha (2)A- and alpha B-2-adrenoceptors and corresponding mRNA are found in kidneys of SBN rats. In these rats, a high-salt diet does not affect blood pressures but increases gene expression and densities of both a2A- and alpha B-2-adrenoceptors. If the up-regulation of renal alpha B-2-adrenoceptor subtypes is indicative of the hypertensive phenotype, the present study shows that this mechanism is also present in normotensive salt-resistant Sabra rats. In fact, the absence of alpha (2)A-adrenoceptors in SBH could be responsible for the lack of adequate receptor-mediated renal functions predisposing to salt-sensitivity and consequently the development of hypertension. Conversely, the presence of this receptor in SBN rats and its up-regulation could be protective change against the increase of alpha B-2-adrenoceptors induced by the salt overload and could consequently be responsible for the resistance to salt-induced hypertension.
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页码:928 / 933
页数:6
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